Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice - 30/10/09
Corresponding author. Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Sagamihara 228-8555, Kanagawa, Japan. Tel.: +81 42 778 8822; fax: +81 42 778 7604.Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Angiotensin II (Ang II) is a bioactive peptide that plays important roles in blood pressure regulation and salt–water homeostasis. Recently, Ang II was reported to function in the promotion of angiogenesis. Since the wound healing process is highly dependent upon angiogenesis, we employed Ang II receptor knockout mice (AT1a−/−) to investigate whether or not Ang II facilitates angiogenesis and wound healing via AT1a receptor signaling. In comparison to wild-type (WT) mice, wound healing and wound-induced angiogenesis were significantly suppressed in AT1a−/− mice, and these mice exhibited reduced expression of CD31 in wound granulation tissues. In comparison to vehicle-treated mice, wound healing was delayed significantly in mice treated with an AT1-R antagonist and this delay was accompanied by the reduced expression of vascular endothelial growth factor in wound granulation tissues. These findings suggest that Ang II–AT1a signaling plays a crucial role in wound healing and wound-induced angiogenesis.
Le texte complet de cet article est disponible en PDF.Keywords : Angiogenesis, Angiotensin II, Wound healing
Plan
Vol 63 - N° 9
P. 627-634 - novembre 2009 Retour au numéro
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